Background The microemboli produced during spontaneous plaque rupture and ulceration and during coronary intervention will reduce coronary reserve and cause cardiac dysfunction. It is though that inflammation caused b...Background The microemboli produced during spontaneous plaque rupture and ulceration and during coronary intervention will reduce coronary reserve and cause cardiac dysfunction. It is though that inflammation caused by the microinfarction induced by the microembolization may play an essential role. It is known that the activation of p38 mitogen-activated protein kinases （MAPK） in both infected and non-infected inflammation in myocardium may cause a contractile dysfunction. But the relation between the activation of p38 MAPK and microembolization is still unknown. Methods Sprague-Dawley rats were randomly divided into three groups： Sham group, coronary microembolization （CME） group and SB203580 group （n=-10 per group）. CME rats were produced by injection of 42 pm microspheres into the left ventricle with occlusion of the ascending aorta. SB203580, a p38 MAPK inhibitor, was injected into the femoral vein after the injection of microspheres to make the SB203580 group. Left ventricular ejection fraction （LVEF） was determined by echocardiography. The protein concentration of P38 MAPK in the myocardium was assessed by Western blotting. The relative expression of mRNA for tumor necrosis factor （TNF）-a was assessed by the technique of semi-quantitative polymerase chain reaction amplification. Results LVEF was depressed at three hours up to 12 hours in the CME group. Increased p38 MAPK activity and TNF-a mRNA expression were observed in the CME group. The administration of SB203580 partly inhibited p38 MAPK activity, but did not fully depress the TNF-α expression, and partly preserved cardiac contractile function. Conclusions p38 MAPK is significantly activated by CME and the inhibition of p38 MAPK can partly depress the TNF-a expression and preserve cardiac contractile function.展开更多
Background The evidence for non-invasive positive pressure ventilation （NIPPV） used in patients with severe stable chronic obstructive pulmonary disease （COPD） is insufficient. The aim of the meta-analysis was to ...Background The evidence for non-invasive positive pressure ventilation （NIPPV） used in patients with severe stable chronic obstructive pulmonary disease （COPD） is insufficient. The aim of the meta-analysis was to assess the treatment effects of long-term NIPPV on gas change, lung function, health-related quality of life （HRQL）, survival and mortality in severe stable COPD patients. Methods Randomized controlled trials （RCTs） and crossover studies comparing the treatment effects of NIPPV with conventional therapy were identified from electronic databases and reference lists from January 1995 to August 2010. Two reviewers independently assessed study quality. Data were combined using Review Manager 5.0. Both pooled effects and 95% confidence intervals were calculated. Results Five RCTs and one randomized crossover study with a total of 383 severe stable COPD patients were included NIPPV improved gas change significantly when using a higher inspiratory positive airway pressures. The weighted mean difference （WMD） for the partial pressure of carbon dioxide in artery （PaCO2） was -3.52 （-5.26, -1.77） mmHg and for the partial pressure of oxygen in artery （PaO2） 2.84 （0.23, 5.44） mmHg. There were significant improvements in dyspnea and sleep quality, but gained no benefits on lung function. The standardized mean difference （SMD） for the forced expiratory volume in 1 second （FEV1） was 0.00 （0.29, 0.29）. And the benefits for exercise tolerance, mood, survival and mortality remained unclear. Conclusions Patients with severe stable COPD can gain some substantial treatment benefits when using NIPPV, especially improvements in gas change, dyspnea and sleep quality. Studies of high methodological quality with large population, especially those based on a higher inspiratory positive airway pressures are required to provide more evidences.展开更多
文摘Background The microemboli produced during spontaneous plaque rupture and ulceration and during coronary intervention will reduce coronary reserve and cause cardiac dysfunction. It is though that inflammation caused by the microinfarction induced by the microembolization may play an essential role. It is known that the activation of p38 mitogen-activated protein kinases （MAPK） in both infected and non-infected inflammation in myocardium may cause a contractile dysfunction. But the relation between the activation of p38 MAPK and microembolization is still unknown. Methods Sprague-Dawley rats were randomly divided into three groups： Sham group, coronary microembolization （CME） group and SB203580 group （n=-10 per group）. CME rats were produced by injection of 42 pm microspheres into the left ventricle with occlusion of the ascending aorta. SB203580, a p38 MAPK inhibitor, was injected into the femoral vein after the injection of microspheres to make the SB203580 group. Left ventricular ejection fraction （LVEF） was determined by echocardiography. The protein concentration of P38 MAPK in the myocardium was assessed by Western blotting. The relative expression of mRNA for tumor necrosis factor （TNF）-a was assessed by the technique of semi-quantitative polymerase chain reaction amplification. Results LVEF was depressed at three hours up to 12 hours in the CME group. Increased p38 MAPK activity and TNF-a mRNA expression were observed in the CME group. The administration of SB203580 partly inhibited p38 MAPK activity, but did not fully depress the TNF-α expression, and partly preserved cardiac contractile function. Conclusions p38 MAPK is significantly activated by CME and the inhibition of p38 MAPK can partly depress the TNF-a expression and preserve cardiac contractile function.
文摘Background The evidence for non-invasive positive pressure ventilation （NIPPV） used in patients with severe stable chronic obstructive pulmonary disease （COPD） is insufficient. The aim of the meta-analysis was to assess the treatment effects of long-term NIPPV on gas change, lung function, health-related quality of life （HRQL）, survival and mortality in severe stable COPD patients. Methods Randomized controlled trials （RCTs） and crossover studies comparing the treatment effects of NIPPV with conventional therapy were identified from electronic databases and reference lists from January 1995 to August 2010. Two reviewers independently assessed study quality. Data were combined using Review Manager 5.0. Both pooled effects and 95% confidence intervals were calculated. Results Five RCTs and one randomized crossover study with a total of 383 severe stable COPD patients were included NIPPV improved gas change significantly when using a higher inspiratory positive airway pressures. The weighted mean difference （WMD） for the partial pressure of carbon dioxide in artery （PaCO2） was -3.52 （-5.26, -1.77） mmHg and for the partial pressure of oxygen in artery （PaO2） 2.84 （0.23, 5.44） mmHg. There were significant improvements in dyspnea and sleep quality, but gained no benefits on lung function. The standardized mean difference （SMD） for the forced expiratory volume in 1 second （FEV1） was 0.00 （0.29, 0.29）. And the benefits for exercise tolerance, mood, survival and mortality remained unclear. Conclusions Patients with severe stable COPD can gain some substantial treatment benefits when using NIPPV, especially improvements in gas change, dyspnea and sleep quality. Studies of high methodological quality with large population, especially those based on a higher inspiratory positive airway pressures are required to provide more evidences.
